Airway smooth muscle is one of the main effectors of bronchial reactivity.
Our understanding of the cellular mechanisms involved in the contraction of
this muscle has advanced in the recent past since isolated cells in cultur
e can now, be studied. Extracellular messengers (neurotransmettors and medi
ators) as well as their specific membrane receptors have been analyzed in s
ome details. Membrane transduction of extracellular messengers brings about
the formation (or the increase in the concentration) of the intracellular
second messager which, in airway smooth muscle, is cytosolic calcium (Ca-i(
2+)) via activation of calcium channels which depend on surface membrane po
tential changes (electro-mechanical coupling) on one hand and mainly via me
chanisms independent of surface membrane potential changes, the so called -
pharmacomechanical coupling - which involves membrane phosphoinositide met
abolism Changes in Ca-i(2+) activate contractile proteins leading the muscl
e to shorten and to develop force via several controlled steps such as phos
phorylation of myosin or changes in the sensitivity to Ca2+ of the contract
ile elements. information about the cellular physiology and pathophysiology
of this muscle is of value to design new drugs for the treatment of bronch
oconstriction.